Abstract： Objective To investigate the protective effects of α-lipoic acid in rats with acute panereatitis(AP)and its potential mechanism.Methods Wistar rats were randomly divided into four groups according to random number table:sham operation(SO)group,AP group,normal saline(NS)group and α- lipoic acid group with 30 rats in each group.AP model was induced by retrograde iniection of 3.5%sodium taurocholate into the pancreatobiliary duct.Rats in α-lipoic acid group immediately received α-lipoic acid intra- peritoneal injection at the dose of 1 mg/kg.Rats in NS group received sanle amount of normal saline.The rats were sacrificed at 1,3,6,9 and 12 h after AP induction.The serunl levels of amylase.TNF-α and ICAM-1 were measured.Pancreatic histological changes were observed.The activities of pancreatic SOD and MDA were measured. Results In rats of AP group,optical microscopy showed pancreatic edema,adhesion and necrosis. The semm amylase,TNF-α,ICAM-1 and MDA levels in pancreatic tissue 6h after operalion were(2211±547)U/L,(174.8±7.9)ng/ml,(49.3±8.0)ng/ml and(32.2±5.9)U/mg prot,respectively,in AP group;which were significantly increased when compared with those of SO group(P<0.05).Pancreatic SOD activity was(38.5±9.5)U/mg prot,which was signifieandy lower than(56.7±6.7)U/mg pint of SO group (p<0.05).The serum amylase,TNF-α,ICAM-1 and MDA levels in pancreatic tissue 6 h after operation in α-lipoic acid group were(1478±642)U/L,(164.8±6.2)ng/ml,(37.5±3.9)ng/ml and(20.2 ±8.4)U/mg prot,respectively;which were significantly decreased when compared with those of AP group(P<0.05).Pancreatic SOD activity was(66.0±8.6)U/mg prot,which were significantly hisher than(38.5±9.5)U/mg prot of AP group(P<0.05).Condusiors The pathogenesis of AP wag associated with oxiddative stress,and α-lipoic acid as an antioxidant played a role in the treatment of AP.the possiblemechanismsincludedinhibitedproduction of TNF-α and ICAM-1.